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肠道微生物群与化脓性汗腺炎之间的因果关系:一项两样本孟德尔随机化研究。

Causal relationship between gut microbiota and hidradenitis suppurativa: a two-sample Mendelian randomization study.

作者信息

Liu Chengling, Liu Xingchen, Li Xin

机构信息

Center of Burns and Plastic Surgery and Dermatology, The 924th Hospital of Joint Logistics Support Force of the PLA, Guilin, China.

Department of Pathology, Changhai Hospital, Naval Medical University, Shanghai, China.

出版信息

Front Microbiol. 2024 Jan 29;15:1302822. doi: 10.3389/fmicb.2024.1302822. eCollection 2024.

DOI:10.3389/fmicb.2024.1302822
PMID:38348190
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10860757/
Abstract

BACKGROUND

Accumulating evidence suggests that alterations in gut microbiota composition are associated with the hidradenitis suppurativa (HS). However, the causal association between gut microbiota and HS remain undetermined.

METHODS

We performed a bidirectional two-sample Mendelian randomization (MR) analysis using genome-wide association study summary data of gut microbiota and hidradenitis suppurativa from the MiBioGen consortium which concluded 18,340 individuals analyzed by the MiBioGen Consortium, comprising 211 gut microbiota. HS data were acquired from strictly defined HS data collected by FinnGenbiobank analysis, which included 211,548 European ancestors (409 HS patients, 211,139 controls). The inverse variance weighted method (IVW), weighted median (WME), simple model, weighted model, weighted median, and MR-Egger were used to determine the changes of HS pathogenic bacterial taxa, followed by sensitivity analysis including horizontal pleiotropy analysis. The MR Steiger test evaluated the strength of a causal association and the leave-one-out method assessed the reliability of the results. Additionally, a reverse MR analysis was carried out to seek for possible reverse causality.

RESULTS

By combining the findings of all the MR steps, we identified four causal bacterial taxa, namely, Family XI, Porphyromonadaceae, group and Lachnospira. The risk of HS might be positively associated with a high relative abundance of group (Odds ratio, OR 2.17,  = 0.00038) and Lachnospira (OR 2.45,  = 0.017) but negatively associated with Family XI (OR 0.67,  = 0.049) and Porphyromonadaceae (OR 0.29,  = 0.014). There were no noticeable outliers, horizontal pleiotropy, or heterogeneity. Furthermore, there was no proof of reverse causation found in the reverse MR study.

CONCLUSION

This study indicates that group and Lachnospira might have anti-protective effect on HS, whereas Family XI and Porphyromonadaceae might have a protective effect on HS. Our study reveals that there exists a beneficial or detrimental causal effect of gut microbiota composition on HS and offers potentially beneficial methods for therapy and avoidance of HS.

摘要

背景

越来越多的证据表明,肠道微生物群组成的改变与化脓性汗腺炎(HS)有关。然而,肠道微生物群与HS之间的因果关系仍未确定。

方法

我们使用来自MiBioGen联盟的肠道微生物群和化脓性汗腺炎的全基因组关联研究汇总数据进行了双向双样本孟德尔随机化(MR)分析,该联盟对18340名个体进行了分析,包括211种肠道微生物群。HS数据来自FinnGen生物银行分析收集的严格定义的HS数据,其中包括211548名欧洲祖先(409名HS患者,211139名对照)。采用逆方差加权法(IVW)、加权中位数(WME)、简单模型、加权模型、加权中位数和MR-Egger法来确定HS致病细菌类群的变化,随后进行包括水平多效性分析在内的敏感性分析。MR Steiger检验评估因果关联的强度,留一法评估结果的可靠性。此外,还进行了反向MR分析以寻找可能的反向因果关系。

结果

综合所有MR步骤的结果,我们确定了四种因果细菌类群,即XI科、卟啉单胞菌科菌群和毛螺菌科。HS的风险可能与菌群的高相对丰度呈正相关(优势比,OR 2.17,P = 0.00038)和毛螺菌科(OR 2.45,P = 0.017),但与XI科(OR 0.67,P = 0.049)和卟啉单胞菌科(OR 0.29,P = 0.014)呈负相关。没有明显的异常值、水平多效性或异质性。此外,在反向MR研究中未发现反向因果关系的证据。

结论

本研究表明,菌群和毛螺菌科可能对HS有抗保护作用,而XI科和卟啉单胞菌科可能对HS有保护作用。我们的研究揭示了肠道微生物群组成对HS存在有益或有害的因果效应,并为HS的治疗和预防提供了潜在的有益方法。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a7dc/10860757/891dc0eec3d3/fmicb-15-1302822-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a7dc/10860757/7bc41bf63e25/fmicb-15-1302822-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a7dc/10860757/2601217d9ca9/fmicb-15-1302822-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a7dc/10860757/a3273ba7f9b0/fmicb-15-1302822-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a7dc/10860757/279898a923a6/fmicb-15-1302822-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a7dc/10860757/4716de4685c3/fmicb-15-1302822-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a7dc/10860757/891dc0eec3d3/fmicb-15-1302822-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a7dc/10860757/7bc41bf63e25/fmicb-15-1302822-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a7dc/10860757/2601217d9ca9/fmicb-15-1302822-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a7dc/10860757/a3273ba7f9b0/fmicb-15-1302822-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a7dc/10860757/279898a923a6/fmicb-15-1302822-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a7dc/10860757/4716de4685c3/fmicb-15-1302822-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a7dc/10860757/891dc0eec3d3/fmicb-15-1302822-g006.jpg

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